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Abuse of anabolic androgenic steroids (AASs) is frequently associated with changes in mood, including depression. However, the nature of this association is still largely unexplored. As a model of AAS abuse, we used male adult rats injected for 4 weeks with either nandrolone or stanozolol at daily doses (5 mg/kg, .) that are considered equivalent to those abused by humans on a milligram per kilogram of body weight basis. AAS treatment reduced levels of brain-derived neurotrophic factor in the hippocampus and prefrontal cortex, reduced the expression of low-affinity glucocorticoid receptors in the hippocampus, and increased morning trough basal plasma corticosterone levels. All these changes have been related to the pathophysiology of major depressive disorder. Accordingly, rats treated with nandrolone or stanozolol showed an increased immobility time in the forced swim test, which is widely used for the screening of antidepressant drugs. All effects produced by AASs were prevented by co-administration with the classical antidepressant, chlorimipramine. The evidence that supraphysiological doses of AASs induce changes indicative of a depressive state in normal rats, raises the concern that AAS abuse in humans may cause depression regardless of exposure to stress or other risk factors.

Results of early studies support the concept that steroid treatment may reduce mortality from acute myocardial infarction. This double-blind, randomized, 1118-patient study was performed to determine if methylprednisolone sodium succinate (MPSS, Solu-Medrol Sterile Powder, The Upjohn Company) reduced 28-day mortality following myocardial infarction complicated by cardiac failure. Treatment with 30 mg/kg intravenous MPSS (maximum dose, 3 g) resulted in 28-day mortality rates of % with MPSS and % with placebo when treatment was initiated within six hours of the onset of chest pain (Group 1). Mortality rates at 28 days were % with MPSS and % with placebo when the treatment was initiated 6-12 hours after onset of chest pain (Group 2). In the late-treatment group, six-month mortality rates were % with MPSS and % with placebo (p = ). Analysis of data by life table methods showed similar survival rates between MPSS- and placebo-treated patients in Group 1. In Group 2, survival rates were increased in MPSS-treated patients in the intervals from 48 hours through seven days (p = ) and from three months through six months (p = ). A Cox regression analysis showed that the relative risk of death for Group 1 patients was similar, regardless of treatment; Group 2 patients on MPSS had a significantly decreased relative risk of death (p less than ). MPSS treatment was not associated with increased incidence of myocardial rupture, cardiac aneurysm, early malignant ventricular arrhythmias, or other adverse cardiac events.

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